Long-term use of angiotensin-converting enzyme inhibitors to modify endothelial dysfunction: a review of clinical investigations.
Bibliographic record
Abstract
OBJECTIVES: Endothelial dysfunction can be modified by angiotensin-converting enzyme (ACE) inhibitors. The purpose of this paper is to review clinical studies assessing the effect of long-term, oral ACE inhibition on endothelial dysfunction in specific disease syndromes and to identify areas requiring further research. DATA SOURCES: A computer search of the entire MEDLINE database and Current Contents complemented by detailed analysis of references in the papers identified. STUDY SELECTION: Analysis of patients treated on a long-term basis with orally administered ACE inhibitors to modify endothelial function. DATA SYNTHESIS: Studies were identified of patients with hypertension, diabetes, congestive heart failure, coronary artery disease, dyslipidemias and immunoglobulin A nephropathy (IgAN). These studies used diverse endothelium-mediated end-points, which included dilatory responses in conduit or resistance vessels, measures of coagulant and fibrinolytic factors, soluble adhesion molecules, endothelin-1, systemic and glomerular barrier functions and renal blood flow. Few trials enrolled large numbers of patients or used randomized, double-blind, placebo-controlled designs. However, consistent and positive effects were noted in patients with coronary artery disease, dyslipidemia or IgAN. In hypertensive patients, conduit artery and renal endothelium-mediated responses could be improved earlier and more easily than resistance vessel function, which appears to require prolonged therapy before improvement is seen. Highly disparate results were found in patients with congestive heart failure or diabetes. CONCLUSIONS: ACE inhibitors appear to improve endothelial dysfunction in patients with coronary artery disease, dyslipidemia, hypertension and IgAN. Conflicting evidence exists in studies of patients with congestive heart failure and diabetes. Further trials are required to clarify and define the prevalence of endothelial dysfunction and the predictors of response in all these conditions.
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.002 | 0.004 |
| Meta-epidemiology (narrow) | 0.001 | 0.000 |
| Meta-epidemiology (broad) | 0.002 | 0.001 |
| Bibliometrics | 0.004 | 0.006 |
| Science and technology studies | 0.000 | 0.001 |
| Scholarly communication | 0.001 | 0.002 |
| Open science | 0.001 | 0.000 |
| Research integrity | 0.001 | 0.001 |
| Insufficient payload (model declined to judge) | 0.003 | 0.001 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".